Smoking and hypoxemia caused by hepatopulmonary syndrome before and after liver transplantation

Severe hypoxemia may occur in patients with liver disease as a result of ab normal intrapulmonary vasodilatations (hepatopulmonary syndrome, HPS). Live r transplantation (LT) is the only effective treatment of HPS, with a quite variable delay of improvement of oxygenation. Smoking, by decreasing respi ratory nitric oxide (NO), apparently contributed to improved oxygenation in a 44-year-old man with alcohol-induced cirrhosis, complicated by HPS, who underwent LT. The patient quit smoking just before LT, when his PaO2 was 29 imn Hg and exhaled NO (eNO) 28 ppb, a value far above the normal limits (9 .6 +/- 3.2 ppb). After LT, oxygenation remained poor and eNO remained high for more than 4 months, when the patient started to smoke again (blood HbCO going up to 5%). At that time eNO decreased to 6 ppb and PaO2 increased to 67 mm. Hg. The strict relationship between eNO and oxygenation observed in this case reinforces the hypothesis that NO is the most important vasodila ting mediator in HPS. Smoking may have hastened the resolution of HPS after LT by inhibiting respiratory NO and/or through a generalized impairment of endothelium-dependent vasodilation.